Voltage-gated ion channels are essential for signal generation and propagation in neurons and other excitable cells. The high-voltage activated calcium-channel Cav2.3 and the calcium- and voltage-gated large conductance potassium channel (BK) are both localized throughout the somato-dendritic region and spines of hippocampal pyramidal neurons. BK channels regulate cellular excitability in various ways, depending on their exact localization and which calcium source provides their gating trigger. Cav2.3 has been shown to provide calcium for other calcium-activated potassium channels, however it has so far been thought that BK channels would not be triggered by R-type calcium current, which is carried by Cav2.3. Here we show that CA1 pyramidal cells which lack Cav2.3 are hyperexcitable and show altered action potential waveforms, which can be traced back to reduced BK-channel function. This change in AP waveform leads to strengthened synaptic transmission between CA1 and the subiculum, resulting in increased short-term plasticity. Our results demonstrate that Cav2.3 impact cellular excitability through BK channels, and likely influences overall hippocampal information processing.